The accumulation of protein fragments
in the brain begins before dementia symptoms start and increases as dementia
becomes more severe, according to the results of a new study.
Based on the findings, which suggest that the accumulation of these
fragments, called amyloid beta-peptides, is to blame for the dementia of
Alzheimer's disease, drugs that remove or block the peptides might help slow
down or even prevent the disease, one of the study's authors told Reuters Health
in an interview.
Two types of abnormal growths in the brain -- plaques made up of amyloid
beta-peptides and tangles composed of tau proteins -- are tell-tale signs of
Alzheimer's disease. But there's been a controversy about which comes first,
plaques or tangles, according to Dr. Paul Greengard of Rockefeller University in
New York. The results of the study, however, appear to place the blame on
plaques.
In the study, Greengard and colleagues performed autopsies on 79 elderly
people, including people who died in various stages of dementia and those
without any mental impairment. The researchers detected elevated levels of two
types of amyloid beta-peptides in the brains of those who had dementia, even
when the diagnosis was in doubt.
And the more severe the dementia, the higher were the levels of amyloid
beta-peptides, according to the report published in The Journal of the American
Medical Association.
Equally as important a finding is what the researchers did not detect. High
levels of amyloid beta-peptides were present even in brains that did not have
any tangles, suggesting that the peptides play the lead role in the development
of dementia.
"The beta amyloid is very probably responsible for the dementia," Greengard
said in the interview. "It's what most of us have thought," he said, but the
study provides important evidence to support the claim. Greengard speculated
that the peptides cause nerve damage that lead to dementia and, in turn, the
formation of plaques and tangles. And even though much of the focus has been on
the collecting of the peptides into plaques, the study shows that high levels of
beta amyloids are present in the brains of people with dementia even before
plaques develop, according to Greengard.
In recent years, there has been a push to develop medications to stop or at
least slow down the progression of Alzheimer's disease by blocking the
production of amyloid beta-peptides, Greengard noted. This study gives drug
companies the assurance "that they're on the right track," he said.
The findings are exciting for this very reason, according to Dr. Dennis J.
Selkoe, of Harvard Medical School in Boston, Massachusetts, author of an
accompanying editorial. In an interview with Reuters Health, Selkoe said that a
risk assessment for Alzheimer's may become a routine part of healthcare within
the next 10 to 15 years.
Beginning when people are in their 40s or 50s, doctors may be able to use
amyloid beta-peptide levels, genetic tests and other measures to determine a
person's risk of developing the disease, he explained. Treatment with drugs that
block the production of amyloid beta-peptides, which are about to be tested in
human trials, might prevent the disease, according to Selkoe.
